In animal studies, ACE2 and AT2R have been shown to protect mice against ARDS caused by acid inhalation or sepsis, while other components of RAAS, such as ACE, angiotensin II and AT1R, can aggravate disease progression and lead to pulmonary edema and lung damage (Imai et al., 2005). The gene discussed is ACE; the disease is acute respiratory distress syndrome.